© 2002 by Oxford University Press
Journal of the National Cancer Institute, Vol. 94, No. 7, 497-504,
April 3, 2002
© 2002 Oxford University Press
ARTICLE |
Hormone Replacement Therapy and the Risk of Invasive Epithelial Ovarian Cancer in Swedish Women
Affiliation of authors: T. Riman, Department of Obstetrics and Gynecology, Falu Hospital, Falun, Sweden, Department of Medical Epidemiology, Karolinska Institute, Stockholm, Sweden, and Department of Women's and Children's Health, Uppsala University, Uppsala, Sweden; P. W. Dickman, N. Correia, C. M. Magnusson, I. R. Persson, Department of Medical Epidemiology, Karolinska Institute; S. Nilsson, Department of Obstetrics and Gynecology, Falu Hospital, and Department of Women's and Children's Health, Uppsala University; H. Nordlinder, Department of Pathology, Uppsala University, and Department of Pathology, Sahlgrenska University Hospital, Gothenburg, Sweden; E. Weiderpass, Department of Medical Epidemiology, Karolinska Institute, Stockholm, and International Agency for Research on Cancer, Lyon, France.
Correspondence to: Tomas Riman, M.D., Department of Obstetrics and Gynecology, Falu Hospital, 79182 Falun, Sweden (e-mail: tomas.riman{at}ltdalarna.se).
Background: Estrogen replacement therapy (ERT), which is mainly used to relieve climacteric symptoms, increases a woman's risk for uterine endometrial cancer and epithelial ovarian cancer (EOC). Estrogens are often combined with progestins in hormone replacement therapy (HRT) to reduce the risk of uterine endometrial cancer. Data on the association between HRT including progestins and EOC risk are limited. This nationwide case–control study examined EOC risk in relation to HRT regimens with sequentially added progestins (HRTsp) and continuously added progestins (HRTcp). Methods: Between 1993 and 1995, we enrolled 655 histologically verified incident case patients with EOC and 3899 randomly selected population controls, all 50–74 years of age. Data on HRT use were collected through mailed questionnaires. Multivariate-adjusted odds ratios (ORs) and 95% confidence intervals (CIs) were estimated by the use of unconditional logistic regression. Results: Risks of EOC were elevated among ever users as compared with never users of both ERT (OR = 1.43, 95% CI = 1.02 to 2.00) and HRTsp (OR = 1.54, 95% CI = 1.15 to 2.05); risks were elevated for serous, mucinous, and endometrioid subtypes. For all EOC types combined, the greatest risk increases were seen with hormone use exceeding 10 years. Ever use of HRTcp was not associated with increased EOC risk relative to HRTcp never use (OR = 1.02, 95% CI = 0.73 to 1.43). The risk of EOC was elevated among HRTsp ever users as compared with HRTcp ever users (OR = 1.78, 95% CI = 1.05 to 3.01). ORs for EOC after ever use of low-potency estrogens were 1.18 (95% CI = 0.89 to 1.55) for oral and 1.33 (95% CI = 1.03 to 1.72) for vaginal applications, but no relationship was seen between EOC risk and duration of use. Conclusion: Ever users of ERT and HRTsp but not HRTcp may be at increased risk of EOC.
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